Inhibition of tumor-induced migration of bovine capillary endothelial cells by mouse and rabbit tumor necrosis factor

• Published in: JNCI : Journal of the National Cancer Institute Vol. 78; no. 1; p. 115
• Main Authors: Mano-Hirano, Y, Sato, N, Sawasaki, Y, Haranaka, K, Satomi, N, Nariuchi, H, Goto, T
• Format: Journal Article
• Language: English
• Published: United States 01.01.1987
• Subjects: Animals; Capillaries - cytology; Cattle; Cells, Cultured; Chemotaxis - drug effects; Culture Media - pharmacology; Depression, Chemical; Endothelium - drug effects; Endothelium - physiology; Glycoproteins - isolation & purification; Glycoproteins - pharmacology; Humans; Meningioma - analysis; Mice; Mice, Mutant Strains; Neovascularization, Pathologic; Rabbits; Sarcoma 180 - analysis; Tumor Necrosis Factor-alpha
• ISSN: 0027-8874
• DOI: 10.1093/jnci/78.1.115

The effect of tumor necrosis factor (TNF) on the tumor-induced endothelial migration was evaluated with the use of a phagokinetic track assay. TNF from both ddy mice and Japanese albino rabbits (sp act, 3-5 X 10(5) U/mg, respectively) was found to inhibit the migration of bovine capillary endothelial (BCE) cells stimulated by factors from tumor cells, such as the medium conditioned with mouse sarcoma 180 cells or human meningioma extract. These TNF preparations, however, did not affect the spontaneous migration of the BCE cells. When mouse TNF was further fractionated by polyacrylamide gel electrophoresis, only TNF-positive fractions showed an inhibitory activity on the tumor-induced endothelial motility. Moreover, monoclonal antibody against rabbit TNF completely neutralized its migration-inhibitory activity. These findings indicate that the observed inhibitory effect of TNF preparations on the endothelial motility evoked by tumor is exclusively ascribed to the function of TNF. This activity presumably is involved in the suppression of tumor angiogenesis in vivo.